Good bugs in our bodies

A new theory suggests that our pitched battle against the microbial world is making us sicker, and possibly fatter.

When a patient is treated with antibiotics, the bad bugs are knocked out, but the drug also attacks many other populations of bacteria that live in our body. And this, it seems, is where the trouble starts.
(Photo: Joe Raedle/Getty Images)

Most of us look at bacteria as the enemy. They are the invisible things that lay in wait all around us — clinging to food, countertops, our hands — ready to ambush us with their ancient poisons.

But many bacteria are our friends, and a new theory suggests that our pitched battle against the microbial world is making us sicker, and possibly fatter.

Antibiotics represent one of medicine’s crowning achievements. They have saved countless lives, and conquered many diseases that once sowed terror.

These miracle drugs are fairly indiscriminate, though. When a patient is treated, the bad bugs are knocked out, but the drug also attacks many other populations of bacteria that live in our body. And this, it seems, is where the trouble starts.

That’s because we are mostly bacteria. In a census of every single cell in our bodies, roughly 9 in 10 of them would turn out to be bacteria. Scientists refer to this as the “microbiome.’’ We are an environment that plays host to microorganisms. Each of us is a world.

It has been known for some time that we depend on this world. Vitamin K, which we rely on for survival, is synthesized by bacteria in our gut. More recently, though, it has become clear that many other bugs are likely good tenants.

“It is not a simple story like bug equals bad,’’ says Dr. Martin Blaser, chair of the Department of Medicine at New York University’s Langone Medical Center. Blaser argues that a long list of serious conditions — among them obesity, asthma, allergies, type 1 diabetes, and inflammatory bowel disease — may be linked to our increased use of antibiotics, and the changes it is causing in our microbiomes.

Blaser first became interested in the topic some three decades ago. In the early 1980s, a pair of Australian scientists proposed that a bacteria called H. pylori in the stomach was responsible for ulcers. It was a strange notion. Ulcers were thought to be a side effect of stress. But the strange notion proved to be fact, and it earned the pair a 2005 Nobel Prize.

H. pylori is common, and this prompted Blaser to wonder what else the H. pylori might be doing in the body. So he looked a bit north, at the esophagus. There he found a link between H. pylori and reflux disease as well as a form of esophageal cancer. But the link was not what you might expect: Those who had the bug were more likely to be healthy, not sick.

From there, Blaser made another leap, to asthma. Again he has shown that people who have H. pylori are less likely to suffer from asthma.

Admittedly, this sounds a bit loony. What could bacteria in the stomach possibly have to do with asthma?

What’s happening in the stomach, it turns out, has far-reaching effects. One recent study found that mice fed bacteria common in many dairy products showed fewer signs of stress and depression. Another showed that mice that do not have normal gut bacteria experience differences in brain development.

Removing species from a natural habitat can have far-reaching effects, and the same appears to be true of the microbiome. For example, farmers have known for decades that feeding low doses of antibiotics to animals makes them heavier. The effect is found in a wide variety of animals, from chickens to sheep, and so it is natural to wonder if the same might be true of humans.

“Maybe giving antibiotics to our kids is fattening them up as well,’’ says Blaser, who has a substantial government grant to investigate this very question.

The use of antibiotics has caused a historic change in our microbiomes, and so, argues Blaser, it is fair to ask what role it might be playing in all the epidemics of our time. Our worlds are out of balance, and the first step is to document the toll.